PMID- 10501206
OWN - NLM
STAT- MEDLINE
DCOM- 19991014
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 73
IP  - 4
DP  - 1999 Oct
TI  - Molecular cloning of a cell cycle regulation gene cyclin H from ischemic rat
      brain: expression in neurons after global cerebral ischemia.
PG  - 1598-608
AB  - Gene expression plays an important role in determining the fate of neurons after 
      ischemia. To identify additional genes that promote survival or execute
      programmed cell death in ischemic neurons, a subtractive cDNA library was
      constructed from hippocampus of rats subjected to global ischemia. With use of a 
      differential screening technique, a cDNA was identified that was up-regulated
      after ischemia. The cDNA was found to have high homology with human cyclin H at
      both the nucleotide level (89%) and the amino acid level (93%). Northern blotting
      detected cyclin H mRNA in nonischemic and ischemic brains. In situ hybridization 
      studies revealed that cyclin H message was found in hippocampal neurons in
      nonischemic brain. After ischemia, expression was increased primarily in the
      dentate gyrus and CA3 regions of hippocampus. Expression of cyclin H protein,
      detected by western blotting of hippocampal tissue, was increased after global
      ischemia, but expression of cyclins B1 and D1 and other related cell cycle genes 
      (Cdk7 and Cdc2) was not increased. Cyclin H immunoreactivity was found
      exclusively within neurons. After ischemia, there was increased immunoreactivity 
      within neurons in dentate gyrus, CA3, and cortex. Thus, cyclin H is expressed in 
      normal postmitotic neurons and expression is increased in neurons that are
      ischemic yet survive. These results suggest that cyclin H may have functions in
      neurons other than cell cycle regulation, including other known functions such as
      DNA repair.
FAU - Jin, K
AU  - Jin K
AD  - Department of Neurology, University of Pittsburgh School of Medicine,
      Pennsylvania 15261, USA.
FAU - Nagayama, T
AU  - Nagayama T
FAU - Chen, J
AU  - Chen J
FAU - Stetler, A R
AU  - Stetler AR
FAU - Kawaguchi, K
AU  - Kawaguchi K
FAU - Simon, R P
AU  - Simon RP
FAU - Graham, S H
AU  - Graham SH
LA  - eng
GR  - NS 24728/NS/NINDS NIH HHS/United States
GR  - P01 NS35965/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (CCNH protein, human)
RN  - 0 (Ccnh protein, rat)
RN  - 0 (Cyclin H)
RN  - 0 (Cyclins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Brain/cytology/*metabolism/pathology
MH  - Cell Cycle/*genetics
MH  - Cloning, Molecular
MH  - Cyclin H
MH  - Cyclins/biosynthesis/chemistry/*genetics
MH  - Humans
MH  - Ischemic Attack, Transient/*metabolism/pathology
MH  - Male
MH  - Molecular Sequence Data
MH  - Neurons/cytology/*metabolism/pathology
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Recombinant Proteins/biosynthesis/chemistry
MH  - Sequence Alignment
MH  - Sequence Homology, Amino Acid
MH  - *Transcription, Genetic
EDAT- 1999/09/29 00:00
MHDA- 1999/09/29 00:01
CRDT- 1999/09/29 00:00
PHST- 1999/09/29 00:00 [pubmed]
PHST- 1999/09/29 00:01 [medline]
PHST- 1999/09/29 00:00 [entrez]
AID - 10.1046/j.1471-4159.1999.0731598.x [doi]
PST - ppublish
SO  - J Neurochem. 1999 Oct;73(4):1598-608. doi: 10.1046/j.1471-4159.1999.0731598.x.